Cardiovascular (CV) toxicity associated with anti-cancer treatment is commonly encountered and raises critical problems that often result in serious morbidity or mortality. Most cardiac toxicities are related to the cumulative dose of chemotherapy; however, the type of chemotherapy, concomitant agents, and/or conventional CV risk factors have been frequently implicated in CV toxicity. Approximately half of the patients exhibiting CV toxicity receive an anthracycline-based regimen. Therefore, serologic biomarkers or cardiac imagings are important during anti-cancer treatment for early detection and the decision of appropriate management of cardiotoxicity. However, given the difficulty in determining a causal relationship, a multidisciplinary collaborative approach between cardiologists and oncologists is required. In this review, we summarize the CV toxicity and focus on the role of cardiac imaging in management strategies for cardiotoxicity associated with anti-cancer treatment.
Biomarkers ; Cardiotoxicity ; Diagnosis* ; Drug Therapy ; Echocardiography* ; Humans ; Mortality ; Risk Factors

Rapid development of anticancer treatments in recent years has greatly improved prognosis of cancer patients. However, with extension of survival time of cancer patients, various short-term and long-term side effects brought about by anticancer treatments, especially cardiotoxicity, have become increasingly prominent. Nonetheless, at present, there is few diagnostic methods with extremely high sensitivity and specificity to detect and accurately predict whether patients with anticancer treatment will experience cardiovascular complications. Inflammation, fibrosis and oxidative stress are considered to be important mechanisms involved in cardiotoxicity anticancer treatments. The cardiovascular biomarkers having the ability to predict and detect cardiovascular dysfunction earlier than clinical symptoms as well as left ventricular ejection fraction monitored by echocardiography, are of great value to timely treatment adjustment and prognosis evaluation. Cardiac troponin T/I and brain natriuretic peptide/N-terminal prohormone of brain natriuretic peptide have been routinely used in clinical practice to monitor cardiotoxicity, and some new biomarkers such as soluble suppression of tumorigenecity-2, myeloperoxidase, growth differentiation factor-15, galectin-3, endothelin-1, have potential in this area. In the future, larger-scale experimental studies are needed to provide sufficient evidences, and how to detect them quickly and at low cost is also a problem to be dealed with.
Biomarkers ; Cardiotoxicity/diagnosis* ; Humans ; Natriuretic Peptide, Brain ; Stroke Volume ; Ventricular Function, Left

BackgroundCardiotoxicity is one of the most serious chronic complications of anthracyclines therapy. Assessment of the left ventricular ejection fraction (LVEF) fails to detect subtle cardiac dysfunction of left ventricular (LV). This study aimed to detect and evaluate new parameters of subclinical anthracyclines' cardiotoxicity in children with solid tumor.

MethodsA detailed echocardiographic examination was performed in 36 children with hepatoblastoma or rhabdomyosarcoma after receiving anthracyclines' chemotherapy and 36 healthy controls from January 2015 to December 2016. The LVEF, ratio of early diastolic peak velocity of transmitral flow (E) and septal diastolic e' mitral annular peak velocity (e'), tricuspid annular plane systolic excursion (TAPSE), and LV global longitudinal strain (GLS) were evaluated using M-mode, tissue Doppler imaging (TDI), and two-dimensional speckle tracking echocardiography (2D-STE), respectively. Echocardiographic parameters were compared between patient group and healthy controls. All patients were divided into two subgroups based on their anthracyclines' cumulative dosage (<300 mg/m subgroup and ≥300 mg/m subgroup).

ResultsAll patients had no presentation of heart failure and LVEF within normal range (65.7 ± 5.1%). Compared with healthy controls, the mean E/e' increased significantly (7.9 ± 0.7 vs. 10.2 ± 3.5, t = 3.72, P < 0.01), mean TAPSE decreased significantly (17.2 ± 1.3 mm vs. 14.2 ± 3.0 mm, t = -4.03, P < 0.01), and mean LV GLS decreased significantly (-22.2% ± 1.9% vs. -17.9% ± 2.9%, t = -5.58, P < 0.01) in patient group. Compared with subgroup with anthracyclines' cumulative dosage < 300 mg/m, mean LV GLS decreased significantly (-18.7 ± 2.7% vs. -16.5 ± 2.1%, t = 2.15, P = 0.04), the mean E/e' increased significantly (9.1 ± 1.5 vs. 11.5 ± 4.9, t = -2.17, P = 0.04), and mean TAPSE decreased significantly (14.2 ± 2.1 mm vs. 12.5 ± 2.2 mm, t = -2.82, P = 0.02) in subgroup with anthracyclines' cumulative dosage ≥300 mg/m.

ConclusionsLV GLS is helpful in the early detection of subclinical LV dysfunction using 2D-STE. E/e' and TAPSE are other sensitive parameters in detecting subclinical cardiac dysfunction of both ventricles by TDI. These parameters show significant change with different anthracyclines' cumulative dosage, so cumulative dosage should be controlled in clinical treatment.

Anthracyclines ; therapeutic use ; Cardiotoxicity ; diagnosis ; Child, Preschool ; Echocardiography ; Female ; Heart Failure ; drug therapy ; pathology ; Humans ; Infant ; Male ; Ventricular Function, Left ; drug effects